{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nWNT3A has emerged as a critical regulator during embryogenesis and adult stem cell fate. In human embryonic and mesenchymal stem cells, WNT3A signaling not only directly induces key transcriptional regulators such as LEF‑1 but also modulates the balance between lineage commitment and proliferation. Studies have shown that WNT3A is dynamically expressed during liver development to promote hepatocyte differentiation, while in pluripotent and mesenchymal stem cells it governs cell-cycle progression, osteoblastogenesis, and even aspects of craniofacial morphogenesis. Moreover, its expression is regulated by factors such as retinoic acid and estradiol, and it can be modulated by extracellular cues that influence growth factor–mediated pathways. These findings together underscore a vital role for WNT3A in coordinating early developmental events and stem/progenitor cell maintenance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "11"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the context of cancer and pathological remodeling, WNT3A exhibits a multifaceted role that can both restrain and reprogram cell phenotypes. In malignant melanoma, for example, activation of WNT3A signaling correlates with increased nuclear β‑catenin, enhanced melanocyte differentiation, and ultimately reduced tumor proliferation and metastatic potential. In several epithelial tumors, including colon cancer, WNT3A‐driven canonical signaling contributes to epithelial–mesenchymal transition and invasiveness; in multiple myeloma, alterations in its paracrine signaling with osteoblasts lead to imbalances in bone turnover. In addition, aberrant production of WNT3A by effector cells has been implicated in altering immune regulation, while in preadipocytes, modulation of its activity (for instance via miR‑103/107) impacts cell survival through endoplasmic reticulum stress pathways. Collectively, these studies reveal that WNT3A not only drives oncogenic signaling in various tumor microenvironments but may also serve as a nodal point in the regulation of EMT, invasion, and inflammatory responses."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "12", "end_ref": "20"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMechanistically, WNT3A functions through the canonical Wnt/β‑catenin pathway by engaging with specific receptor complexes and modulating a variety of downstream effectors. Reconstitution studies have delineated the assembly of the Fz receptor cysteine‐rich domain with LRP6 in the presence of WNT3A, while its activity is finely tuned by regulatory kinases such as CKI isoforms and by deubiquitinating enzymes (for example, CYLD) that affect the stability and polymerization of cytoplasmic effectors like Dishevelled. The structural integrity of WNT3A, governed by critical disulfide bonds, is essential for its ligand–receptor interactions, and its signaling output can be further modulated by mechanosensory cues (via primary cilia) and by cofactors such as TAZ during osteogenic differentiation. These insights into the molecular composition and regulation of the WNT3A signaling cascade not only advance our understanding of its diverse biological functions but also highlight potential therapeutic targets for modulating aberrant Wnt activity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "21", "end_ref": "28"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Masaru Katoh "}, {"type": "b", "children": [{"type": "t", "text": "Regulation of WNT3 and WNT3A mRNAs in human cancer cell lines NT2, MCF-7, and MKN45."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Int J Oncol (2002)"}]}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "11788904"}], "href": "https://pubmed.ncbi.nlm.nih.gov/11788904"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Mohammed Filali, Ningli Cheng, Duane Abbott, et al. 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